Reprinted with permission from Brain Energy by Christopher M. Palmer, MD (BenBella Books, Inc., 2022)
What we eat, When we eat, and how much we eat have direct effects on metabolism and mitochondria. Everyone knows that diet plays a role in obesity, diabetes, and cardiovascular disease. What most people may not realize is that diet also has profound effects on mental health and the brain.
This field is huge. Tens of thousands of research articles and countless textbooks have explored the effects of diet on metabolism and mitochondria. Most of this research has focused on obesity, diabetes, cardiovascular disease, Alzheimer’s disease, aging, and longevity. However, these researchers often fail to see the connection to mental health.
Connections go far beyond correlations. They overlap at the level of neural circuitry in the brain and, of course, the entire network of metabolism and mitochondria within the human body. For example, the neural circuits that drive appetite and eating behaviors have also been directly implicated in addiction to tobacco, alcohol, and heroin. That’s not too surprising to most people. What might be more surprising is that the neural circuitry for loneliness directly overlaps with the neural circuitry that warns of hunger. This study, published in Natureshowed that chronic social isolation in the fruit fly led to increased feeding Y decreased sleep. A “social” problem caused changes in appetite and sleep. When the researchers artificially stimulated the neural circuitry for social isolation, the flies ate more and slept less. Another study identified specific GABA and serotonin neural circuits that were directly involved in obesity. Y anxiety and depression. Neural circuitry plays a role in how much you weigh Y how does it feel
Some people call this field nutritional psychiatry, one that looks at the role of diet in mental health. Personally, I think this is too narrow. It’s more than how diet affects brain function. It’s also about how our mental states affect our metabolism, which can affect appetite and eating behavior, which can affect overall health. It is a two-way relationship. Metabolic affects mental and mental affects metabolic.
There are at least seven different ways that dietary interventions can be helpful in addressing mental symptoms:
- Address nutritional deficiencies, such as folate, vitamin B12, and thiamine deficiency.
- Elimination of dietary allergens or toxins. For example, some people have an autoimmune disorder called celiac disease that causes inflammation and other metabolic problems in response to gluten. This can also affect brain function. I have described the toxic effects of TFA. There are many other dietary ingredients that can also affect mitochondrial function.
- Eating a “healthy diet,” such as the Mediterranean diet, may play a role for some people.
- Improvement of the intestinal microbiome.
- Improve metabolism and mitochondrial function with a dietary intervention. This includes changes in insulin resistance, metabolic rate, the number of mitochondria in cells, the overall health of mitochondria, hormones, inflammation, and many other known regulators of metabolism.
- Losing weight can help alleviate the problems associated with obesity.
- Weight gain can be a life-saving intervention for those who are very underweight.
There is also evidence that fasting, intermittent fasting (IF), and fasting-mimicking diets may play a role in the treatment of mental disorders. All result in the production of ketone bodies, which are produced when fat is used as an energy source. Fat is converted to ketones. And interestingly, this process occurs exclusively in the mitochondria, yet another role for these magnificent organelles.
We have evidence that IF improves mood, cognition, and protects neurons from damage in animal models of epilepsy and Alzheimer’s disease. A group of researchers set out to understand how and why. You’ll never guess what they found: they’re mitochondria! The researchers put the mice through an IF routine. They found that the hippocampus, a brain region often implicated in depression, anxiety and memory disorders, largely drove the improvements in IF. It seemed to be mainly due to higher levels of GABA activity, which reduced hyperexcitability. The researchers then went further to understand what was causing this change in GABA activity. They removed Sirtuin 3 from the mice in two different ways. This protein is unique and essential for mitochondrial health. When they did this, all benefits were lost. This clearly implicates mitochondria directly in the brain health benefits of IF.